Ophthalmology

Ophthalmology • Common eye conditions • Emergency medicine study note Scleral Disorders: Episcleritis, Scleritis, Scleral Thinning and Emergencies Scope. The sclera is the tough, collagen-rich outer coat of the eye. Inflammation may be superficial and self-limiting (episcleritis), or deep, destructive and vision-threatening (scleritis). The two can look similar at first glance, but their pain, colour, vessel pattern, systemic associations, complications and treatment are very different. This resource expands the supplied teaching slides into a practical guide for emergency medicine and ophthalmology learners. Emergency principle: a very painful red eye, pain on eye movement, reduced vision, deep violaceous injection, scleral tenderness, proptosis, hypopyon, trauma, recent ocular surgery or immunosuppression should be treated as possible scleritis, keratitis, uveitis, endophthalmitis or orbital disease. Check visual acuity and pupils immediately, avoid pressure on a possibly thin or open globe, and arrange same-day ophthalmic assessment. Learning objectives Describe scleral anatomy, blood supply and the relationship between sclera, episclera, conjunctiva, cornea and uvea. Differentiate episcleritis from scleritis and from conjunctivitis, keratitis, uveitis and acute glaucoma. Classify anterior, posterior, diffuse, nodular, necrotising and infectious scleritis. Recognise systemic inflammatory, infectious, traumatic, postoperative and drug-related causes. Perform a safe assessment, choose focused investigations and begin appropriate emergency management and referral. Anticipate complications such as keratitis, uveitis, glaucoma, cataract, retinal detachment, scleral melt and perforation. 1. Anatomy and physiology of the sclera The sclera forms approximately the posterior five-sixths of the fibrous coat of the globe. It is continuous anteriorly with the cornea at the limbus and posteriorly with the dura surrounding the optic nerve. Its dense, irregular type-I collagen gives the eye shape and protects the intraocular contents while allowing the extraocular muscles to insert and move the globe. Layer/structure Function Clinical relevance Conjunctiva Transparent mucous membrane over the anterior sclera. Diffuse superficial redness and discharge favour conjunctival disease; it can move over the deeper scleral vessels. Episclera Loose, vascular connective tissue between conjunctiva and sclera. Inflammation produces episcleritis, usually sectoral, bright red and mildly tender. Sclera Dense collagenous coat; avascular-looking deep tissue nourished by episcleral and choroidal circulation. Inflammation is deep, painful and violaceous; prolonged disease weakens or thins the wall. Tenon capsule Fascial sheath around the globe that permits smooth ocular movement. Inflammation may mimic orbital pain or restrict movement; posterior disease can cause exudative retinal detachment. Limbus Transition between corneal and scleral tissues with corneal epithelial stem cells. Ciliary flush or limbal involvement may indicate keratitis, anterior uveitis or severe scleritis rather than simple surface redness. Although the sclera itself has relatively few vessels, inflammation recruits deep and superficial vascular networks. This explains why the eye can appear intensely red even when the primary pathology is not conjunctival. The posterior sclera lies close to the choroid, retina, optic nerve and extraocular muscles, so posterior inflammation can reduce vision without an obvious anterior red eye. 2. A safe approach to the painful red eye 2.1 History Onset and course: sudden, progressive, recurrent, migratory or chronic symptoms; ask about previous episodes and the duration of pain before redness. Pain quality: deep boring or aching orbital pain, pain radiating to the face or temple, pain on eye movement and night pain favour scleritis. Mild irritation and tenderness favour episcleritis. Vision: ask about blur, field loss, floaters, flashes, halos, colour desaturation and diplopia. Any new reduction is a red flag. Photophobia and discharge: prominent photophobia suggests corneal or uveal involvement; watery discharge may accompany scleritis, while purulent discharge suggests infection. Systemic inflammatory symptoms: joint pain or morning stiffness, back pain, psoriasis, inflammatory bowel disease, painful ears or nose, oral/genital ulcers, sinus disease, cough, haematuria, skin purpura and neuropathy. Infection and exposure: tuberculosis, syphilis, herpes zoster, fungal infection, recent respiratory or skin infection, bites, contaminated water, surgery, injections and penetrating trauma. Medication history: bisphosphonates, topical glaucoma medicines, immune-checkpoint inhibitors, anticoagulants and recent corticosteroid withdrawal; ask about allergy and immunosuppression. Trauma/operation: previous pterygium or cataract surgery, scleral buckle, foreign body, chemical burn or recent intraocular procedure can predispose to infectious or necrotising disease. 2.2 Examination sequence Assess general condition, temperature, facial rash, ear/nose cartilage, joint swelling and signs of systemic vasculitis. Measure visual acuity in each eye separately with correction and pinhole. Record the baseline before treatment. Inspect pupils, colour vision if available, and check for a relative afferent pupillary defect. Assess ocular motility, pain on movement, diplopia, proptosis and restriction, which may indicate posterior scleritis or orbital disease. Compare the hue and distribution of injection. Episcleral vessels are bright red or salmon-pink and often sectoral; scleritis is deeper, diffuse or nodular and violaceous. Observe whether vessels move with a cotton bud and whether superficial vessels blanch with a clinician-administered vasoconstrictor test. Never delay referral or use a test as a substitute for slit-lamp examination. Examine the cornea with fluorescein for ulcer, infiltrate, thinning, melt or a Seidel leak. Do not press on a suspected perforation or severely thinned sclera. Examine the anterior chamber for cells, flare, hypopyon and fibrin; examine the lens, vitreous and fundus when possible. Measure intraocular pressure only after an open globe has been excluded and when the examination is safe. Palpate the globe gently only if there is no concern for perforation; document focal tenderness, nodules, scleral thinning and areas of translucency. High-risk findings needing same-day ophthalmology: severe deep pain, pain on eye movement, reduced vision, photophobia with anterior chamber inflammation, corneal ulcer or thinning, violaceous or necrotising sclera, scleral nodule, proptosis, diplopia, hypopyon, recent surgery/trauma, immunosuppression, suspected infection or failure of presumed episcleritis to settle. 3. Episcleritis Episcleritis is inflammation of the superficial episcleral tissue. It usually affects young or middle-aged adults, is often idiopathic and frequently recurs. It can be associated with rheumatoid arthritis, inflammatory bowel disease, systemic lupus, gout, rosacea, vasculitis and other immune conditions, but most patients do not have a serious systemic illness. 3.1 Clinical patterns Pattern Appearance and symptoms Typical course Simple episcleritis Sectoral or diffuse bright-red injection, mild tenderness, watering, gritty sensation and little or no photophobia. Often resolves spontaneously over days to a few weeks. Nodular episcleritis Localised,

Ophthalmology • Common eye conditions • Emergency medicine study note Disorders of the Conjunctiva: Conjunctivitis, Trachoma, Pterygium and Other Conditions Scope. The conjunctiva is a visible, vascular mucous membrane, so many systemic, infectious, allergic, traumatic and neoplastic processes first appear as a “red eye.” This resource brings together the major conjunctival disorders, the history and examination needed to separate a simple conjunctivitis from sight-threatening disease, and a safe management pathway for emergency and primary-care learners. It expands the supplied teaching slides with clinical reasoning, public-health practice and referral thresholds. Safety note: A red eye with severe pain, photophobia, reduced vision, corneal opacity, fixed or irregular pupil, proptosis, trauma, chemical exposure, contact-lens use, neonatal discharge or systemic toxicity is not “just conjunctivitis.” Measure visual acuity urgently, protect the eye, avoid unsupervised steroid drops and arrange same-day ophthalmic assessment. If chemical injury is possible, irrigate immediately before completing the examination. Learning objectives Describe conjunctival anatomy, physiology and the clinical meaning of follicles, papillae, chemosis and injection. Classify infectious, allergic/immune, irritative, degenerative, haemorrhagic, traumatic and neoplastic disorders. Take a focused red-eye history and perform an examination that does not miss keratitis, uveitis, acute glaucoma or orbital disease. Give appropriate first aid, infection-control advice, treatment principles, safety-netting and referral. Recognise trachoma and other conditions in which prevention and community action protect vision. 1. Anatomy and physiology The conjunctiva is a thin, transparent mucous membrane lining the posterior eyelids and covering the anterior sclera. It is continuous with the epithelium of the eyelid margin and joins the corneal epithelium at the limbus. Part Location and function Clinical relevance Palpebral (tarsal) conjunctiva Firmly attached to the inner upper and lower lids; contains vessels, lymphoid tissue and goblet cells. Follicles, papillae, foreign bodies and giant papillae may be most obvious here; evert the upper lid when safe. Forniceal conjunctiva Loose folds joining lid and globe; permit ocular movement and form a cul-de-sac for tears and topical medication. Retained foreign material, scarring and symblepharon can hide here. Bulbar conjunctiva Moves over the sclera and is loosely attached except near the limbus; normally white or lightly vascular. Diffuse injection, chemosis, subconjunctival haemorrhage, pinguecula and pterygium are seen here. Limbal transition Conjunctiva meets cornea at the limbus, where stem cells maintain corneal epithelium. Ciliary flush, limbal follicles or infiltrates suggest corneal, uveal or severe inflammatory disease rather than uncomplicated conjunctivitis. Goblet cells produce mucins that allow the aqueous tear layer to spread over the cornea. Conjunctival vessels provide immune surveillance and become dilated in inflammation. Lymphatics drain to preauricular and submandibular nodes. The conjunctiva is therefore a barrier, a lubricating surface and an immunological organ, not merely a “covering.” 2. The red-eye approach: triage before labels 2.1 Focused history Time course: sudden (minutes to hours), acute (days), recurrent or chronic (weeks/months). Laterality: unilateral onset that spreads to the other eye suggests contagious viral disease; bilateral simultaneous symptoms suggest allergy, irritant exposure or systemic disease. Vision: ask what has changed, whether it is corrected by blinking, and whether there is a field defect, halos or diplopia. Reduced acuity is a red flag. Pain and photophobia: itch and gritty discomfort favour conjunctiva; deep pain, marked photophobia or pain when light is shone in the unaffected eye suggests cornea, uvea or glaucoma. Discharge: watery (viral, allergic, irritant), mucoid/stringy (allergy), mucopurulent (bacterial) or copious hyperpurulent discharge (gonococcal emergency). Exposure and risk: sick contacts, school or household outbreak, swimming pool, dust/chemical splash, cosmetics, topical medicines, contact lenses, sexual exposure, newborn age, trauma and retained foreign body. Medical context: atopy, asthma/eczema, autoimmune disease, HIV or other immunosuppression, diabetes, anticoagulants, recent surgery, sexually transmitted infection and prior herpes. Recurrence or scarring: recurrent episodes, trichiasis, photophobia and declining vision require assessment for trachoma, cicatrising conjunctivitis or ocular-surface disease. 2.2 Examination sequence Check general appearance, fever, facial/orbital swelling, vesicles and ability to open the eye. Measure and document visual acuity in each eye separately, with usual correction and a pinhole if available. Inspect pupils for size, reactivity and a relative afferent pupillary defect; assess ocular motility and diplopia. Use a bright light to compare diffuse conjunctival injection with a deeper violaceous ciliary flush around the limbus. Inspect lids and lashes; look for vesicles, crusting, ectropion, entropion, trichiasis and swelling. Evert the upper lid when a tarsal foreign body is suspected and there is no open-globe concern. Characterise discharge, chemosis, follicles (round, pale elevations) and papillae (polygonal elevations with a central vessel). Instil fluorescein when appropriate and examine with cobalt-blue light: epithelial defects, dendritic lesions, ulcers, foreign-body tracks and Seidel leakage must be identified. Examine cornea, anterior chamber and lens. A hazy cornea, hypopyon, cells/flare or irregular pupil is an ophthalmic emergency. Palpate preauricular and submandibular nodes. A tender preauricular node supports viral, chlamydial or severe bacterial disease. Measure intraocular pressure only when it is safe and an open globe has been excluded; never press on a suspected penetrating injury. Same-day/same-hour referral: visual loss, severe or deep pain, marked photophobia, corneal opacity or ulcer, fluorescein dendrite, hypopyon, irregular/fixed pupil, proptosis or restricted motility, contact-lens red eye, suspected gonococcal disease, neonatal purulent discharge, chemical injury, penetrating trauma, recurrent cicatrising disease, or failure to improve as expected. 3. Infectious conjunctivitis 3.1 Viral conjunctivitis Adenoviruses cause highly contagious pharyngoconjunctival fever and epidemic keratoconjunctivitis (EKC). It usually begins in one eye and reaches the other within days. Watery discharge, gritty discomfort, follicular reaction, preauricular lymphadenopathy, sore throat and fever are typical. EKC may involve the cornea and cause prolonged photophobia and reduced vision. Transmission: hands, towels, respiratory droplets and contaminated examination equipment. Virus can persist on surfaces. Examination: watery discharge, follicles, chemosis, tender preauricular node and sometimes punctate keratitis or subepithelial infiltrates. Management: hand hygiene, separate towels, avoid eye touching, clean discharge with clean water or saline, lubricating drops and cool compresses. Stop contact lenses and eye cosmetics until completely recovered. Antibiotics: do not treat routine viral disease; they do not shorten adenoviral illness and can cause allergy or resistance. Steroids: topical corticosteroids may temporarily improve severe inflammation but can prolong adenovirus, worsen

Common Eye Conditions • Lacrimal apparatus • Watering eye and dacryocystitis Disorders of the Lacrimal Apparatus: Watering Eye, Obstruction and Dacryocystitis The lacrimal apparatus produces, spreads and drains the tear film. Disorders may present with watering, discharge, recurrent conjunctivitis, medial canthal swelling or painful infection. The emergency clinician must distinguish reflex tearing from drainage obstruction and identify dacryocystitis that has extended to preseptal/orbital cellulitis. Emergency warning: Fever with medial-canthal swelling, proptosis, painful/restricted eye movements, reduced vision, RAPD, severe headache, vomiting, altered consciousness, rapidly spreading facial swelling or neonatal dacryocele requires urgent hospital/ophthalmic assessment. Learning objectives Describe the lacrimal glands, puncta, canaliculi, lacrimal sac and nasolacrimal duct. Explain epiphora and differentiate overproduction from drainage failure. Recognise congenital/acquired nasolacrimal obstruction, canaliculitis, dacryocystitis and dacryoadenitis. Perform a safe history and examination, including medial-canthus and nasal assessment. Describe first aid, medical treatment, investigations, definitive procedures and prevention. Recognise complications requiring admission and urgent specialist referral. 1. Anatomy and physiology of tears Structure Role Clinical relevance Main lacrimal gland Produces the aqueous component of the tear film; located superotemporally in the orbit. Inflammation causes painful superotemporal swelling and reduced tear production. Accessory lacrimal glands Contribute baseline aqueous secretion. Support continuous surface lubrication. Conjunctival goblet cells Produce mucin that helps tears spread over epithelium. Surface disease can cause unstable tears and reflex watering. Meibomian glands Produce lipid layer that reduces evaporation. Dysfunction causes evaporative dry eye and reflex tearing. Upper/lower puncta Small openings at the medial lid margins that collect tears. Ectropion, scarring or stenosis causes epiphora. Canaliculi Short channels from puncta to the lacrimal sac; common canaliculus may join before the sac. Canaliculitis, concretions and trauma can obstruct flow. Lacrimal sac Reservoir in the lacrimal fossa between the medial canthal tendon and nasal bone. Stasis and infection cause dacryocystitis and medial-canthal swelling. Nasolacrimal duct Carries tears through the bony canal to the inferior nasal meatus. Congenital membrane or acquired stenosis causes chronic watering/infection. Blinking creates a lacrimal pump: orbicularis contraction compresses the canaliculi and sac, while lid apposition directs tears toward the puncta. A normal tear system therefore depends on secretion, a smooth ocular surface, correct lid position, patent drainage and nasal anatomy. 2. Watering eye (epiphora) Epiphora means tears overflow onto the cheek. It may be caused by excessive reflex production, failure of drainage or both. Ask whether the eye is truly watering or feels dry with intermittent reflex tearing. Mechanism Examples Clues Reflex overproduction Dry eye, blepharitis, allergy, foreign body, corneal abrasion/ulcer, keratitis, smoke/wind/chemical irritation. Burning, gritty sensation, redness, photophobia or pain. Punctal problem Punctal stenosis/atresia, ectropion, scarring or inflammation. Overflow with abnormal punctum position or lid malposition. Canalicular obstruction Canaliculitis, concretions, trauma, surgery, inflammation. Medial lid tenderness, pouting punctum, discharge or recurrent unilateral symptoms. Sac/duct obstruction Primary acquired NLDO, congenital obstruction, tumour, trauma, chronic inflammation. Persistent unilateral watering, reflux from punctum or recurrent dacryocystitis. Nasal cause Rhinitis, inferior-meatus obstruction, polyps, sinus disease or fracture. Nasal congestion, discharge, bleeding or prior nasal trauma/surgery. 3. History and examination Record onset, laterality, constant/intermittent pattern and whether tears run down the cheek. Ask about pain, redness, discharge, fever, trauma, surgery, nasal disease, contact lenses and systemic inflammatory disease. Check vision, pupils/RAPD, cornea, conjunctiva, eyelid position and ocular motility. Inspect the puncta for position, stenosis, pouting, concretions and discharge. Palpate gently over the lacrimal sac, noting tenderness, swelling and reflux; do not force pressure in acute infection. Examine the nose for congestion, purulence, bleeding, mass, septal disease and inferior-meatus obstruction. Assess the medial canthus and orbit for proptosis, spread, skin necrosis or painful movements. 4. Nasolacrimal duct obstruction (NLDO) Congenital obstruction Congenital NLDO commonly results from persistence of a distal membranous barrier near the inferior nasal meatus. Infants present with persistent tearing and mucous mattering despite otherwise healthy eyes. Complications include recurrent infection, dacryocele and rarely orbital/airway problems. Check the red reflex, cornea, pupil and visual behaviour so congenital glaucoma, cataract and corneal disease are not missed. Clean discharge with sterile saline/gauze; avoid sharing towels. In uncomplicated infants, clinicians may teach gentle lacrimal-sac massage and monitor. Recurrent infection, dacryocele, fever or corneal/visual abnormality requires paediatric ophthalmology. Persistent obstruction may require probing or other lacrimal intervention by an ophthalmologist; acute infection is treated first. Acquired obstruction Cause Examples Clinical clues Primary acquired stenosis Inflammatory/fibrotic narrowing, often in older adults. Chronic unilateral epiphora, recurrent discharge or dacryocystitis. Traumatic/iatrogenic Medial eyelid injury, facial fracture, nasal/ocular surgery. Onset after trauma/procedure; canalicular or punctal injury. Infectious/inflammatory Chronic conjunctivitis, canaliculitis, sarcoidosis, granulomatosis or autoimmune disease. Recurrent inflammation, bloody reflux or systemic symptoms. Neoplastic Lacrimal sac/nasal tumour. Blood-stained tears, firm mass, unilateral persistent symptoms or failure of usual treatment. Medication/radiation Chronic topical toxicity, chemotherapy or radiotherapy. Dry eye plus stenosis or history of treatment. 5. Dacryocystitis Dacryocystitis is infection and inflammation of the lacrimal sac, usually because nasolacrimal obstruction causes tear stasis. It may be acute, chronic or recurrent. Type Features Risks Acute Rapid painful erythema, warmth and swelling over the inferomedial canthus; tearing, discharge and tenderness. Abscess, preseptal/orbital cellulitis, fistula, sepsis and intracranial spread. Chronic Persistent watering, mucous discharge, medial swelling and reflux with pressure. Recurrent conjunctivitis, corneal contamination and acute flares. Congenital/neonatal Dacryocele or medial canthal swelling with tearing/discharge. Rapid infection, orbital cellulitis, meningitis or airway compromise in severe cases. Clinical distinction In dacryocystitis, the maximal tenderness is over the lacrimal sac below/near the medial canthus; the punctum may look relatively normal. In canaliculitis, the punctum/canaliculus is pouting, red and tender, and concretions or discharge may express. In orbital cellulitis, proptosis, painful restricted motility, diplopia, reduced vision or RAPD indicate postseptal spread. Management principles Assess severity: vitals, vision, pupils, motility, proptosis, fever, neurological status and immunocompromise. Uncomplicated acute disease: warm compresses and clinician-directed systemic antimicrobial treatment with close review; culture purulent material when appropriate. Abscess: urgent ophthalmic drainage may be required. Avoid forceful massage or probing through friable infected tissue. Complicated disease: admission, IV antibiotics, imaging and surgical consultation if orbital signs, systemic toxicity, immunosuppression, rapid progression or failure of oral therapy. Definitive treatment: after acute inflammation settles, address obstruction—often with

Common Eye Conditions • Eyelid disorders • Emergency-medicine learning resource Disorders of the Eyelids: Ectropion, Entropion, Blepharitis and Styes The eyelids protect the cornea, spread the tear film, remove debris and regulate light. Disorders of their skin, glands, muscles, margin or position can cause pain, tearing, dryness, recurrent infection and corneal damage. In emergency medicine, an apparently small lid lesion may coexist with an open-globe injury, orbital trauma, canalicular damage or exposure keratopathy. Examine the globe and vision before treating the lid alone. Emergency warning: Reduced vision, severe pain, photophobia, corneal opacity, proptosis, painful/restricted eye movements, an irregular pupil, lid laceration with fat prolapse or medial-canthus injury, chemical exposure, rapidly spreading swelling, fever or inability to close the eye requires urgent ophthalmic assessment. Learning objectives Describe eyelid anatomy and the protective functions of blinking, the lid margin and meibomian glands. Classify and recognise ectropion, entropion, blepharitis, hordeolum (stye), chalazion, ptosis, trichiasis, lagophthalmos and eyelid trauma. Differentiate common benign lid disease from preseptal/orbital cellulitis and sight-threatening corneal disease. Take a focused history and perform a safe external eye examination. Provide first aid, medical treatment principles, referral criteria, nursing care and prevention. 1. Eyelid anatomy and physiology Structure Function Clinical relevance Skin and orbicularis oculi Thin protective covering; orbicularis closes the lids and drives blinking. Facial-nerve palsy or scarring may cause lagophthalmos and exposure keratopathy. Tarsal plates Dense connective framework that gives lids shape. Contain meibomian glands; injury can distort the lid margin. Meibomian glands Secrete lipid that reduces tear evaporation. Dysfunction contributes to dry eye, blepharitis and chalazion. Lash follicles/Zeis and Moll glands Protective lashes and associated sebaceous/apocrine glands. Infection can produce an external hordeolum. Conjunctival fornices Allow lid and globe movement and retain tear film. Foreign bodies may hide in the superior fornix. Levator palpebrae and superior tarsal muscle Elevate upper lid through CN III and sympathetic contributions. Ptosis may indicate nerve, muscle, tendon or mechanical disease. Lacrimal puncta Drain tears from the medial lid margin. Ectropion, trauma or inflammation can cause watering. 2. Assessment of a patient with eyelid disease Stabilise: check airway, breathing, circulation, neurological status and severe systemic infection first. Ask about onset and progression: hours/days versus chronic; recurrent versus first episode. Check sight: visual acuity each eye, pupils/RAPD, visual fields when indicated and colour if optic-nerve disease is suspected. Assess pain and inflammation: surface pain, deep pain, photophobia, fever, headache, nausea/vomiting and pain on movement. Inspect both lids: position, margin, lashes, swelling, wounds, crusts, nodules, skin disease, closure and symmetry. Examine the globe: conjunctiva, cornea, anterior chamber, pupil, motility and proptosis; never assume the lid is the whole problem. Consider risk factors: diabetes, immunosuppression, rosacea, seborrhoeic dermatitis, eczema, contact lenses, trauma, surgery and topical medicines. 3. Eyelid malposition Entropion Entropion is inward rotation of the eyelid margin, usually the lower lid, causing lashes and skin to rub against the ocular surface. It can be involutional (age-related), cicatricial (scarring), spastic or congenital. Cause Mechanism Clues Involutional Lid laxity, orbicularis override and weakening of retractors. Older adult, intermittent inward turning, worse with squeezing. Cicatricial Shortening/scarring of the posterior lamella or conjunctiva. Trachoma, chemical injury, burns, autoimmune mucous-membrane disease or surgery. Spastic Orbicularis spasm triggered by painful ocular-surface disease. Acute blepharospasm and secondary entropion. Congenital Developmental lid configuration. Child with lash contact; distinguish from epiblepharon. Symptoms/signs: foreign-body sensation, tearing, photophobia, redness, recurrent abrasions, trichiasis and corneal ulceration. Inspect the cornea with fluorescein and document visual acuity. Ectropion Ectropion is outward eversion of the lid margin, most often the lower lid. The punctum may no longer contact the tear lake, causing epiphora, and the exposed conjunctiva/cornea may dry. Cause Examples Complications Involutional Age-related horizontal laxity. Watering, exposure and chronic conjunctivitis. Paralytic Facial-nerve (CN VII) palsy. Lagophthalmos and exposure keratopathy. Cicatricial Burns, trauma, skin disease, surgery or scarring. Progressive exposure and corneal damage. Mechanical Tumour, oedema or heavy lid lesion. Malposition improves only when the cause is addressed. Symptoms/signs: excessive tearing, dryness, irritation, visible everted punctum, conjunctival exposure and incomplete closure. Check facial movement and corneal staining. 4. Blepharitis Blepharitis is chronic or recurrent inflammation of the eyelid margins. It may be anterior, posterior or mixed. Causes include bacterial colonisation, seborrhoeic dermatitis, rosacea, atopy, meibomian-gland dysfunction, Demodex infestation, allergy and medication irritation. Chronic unilateral disease with lash loss or an atypical mass requires assessment for masquerading tumour or autoimmune scarring disease. Type Main site/features Associations Anterior staphylococcal Crusts/collarettes at lash bases, lid-margin erythema, recurrent styes. Bacterial colonisation, chronic inflammation. Anterior seborrhoeic Greasy scales, dandruff and mild redness. Seborrhoeic dermatitis. Posterior/meibomian Plugged glands, thick secretions, lid-margin telangiectasia and tear-film instability. Rosacea, meibomian-gland dysfunction, evaporative dry eye. Demodectic Cylindrical dandruff/collarettes and recurrent irritation. Demodex overgrowth; may be chronic and refractory. Contact/allergic Itching, oedema, dermatitis and burning after a product/drop. Cosmetics, preservatives, topical medication or atopy. Symptoms and signs Burning, itching, grittiness, foreign-body sensation, crusting and fluctuating blur. Red/swollen lid margins, collarettes, capped meibomian glands and abnormal tear film. Dry-eye symptoms, recurrent hordeola/chalazia, conjunctival injection and corneal punctate staining. Severe pain, reduced acuity, marked photophobia, corneal infiltrate or proptosis is not typical uncomplicated blepharitis and needs urgent reassessment. Management Lid hygiene: warm (not scalding) compresses for several minutes, gentle lid massage toward the margin and careful cleaning of crusts; continue long-term even after symptoms improve. Surface support: preservative-free lubricants when dry eye coexists; manage environmental triggers and blinking. Underlying skin disease: treat seborrhoeic dermatitis, rosacea or atopy with the appropriate clinician. Medicines: topical antibiotic ointment or short anti-inflammatory treatment may be used for selected cases under local/ophthalmic protocol. Oral tetracycline-class therapy may be considered by specialists for significant meibomian/rosacea disease; account for pregnancy, age, allergy and interactions. Demodex: specialist-directed lid therapy may be required; avoid unapproved household products near the eye. Follow-up: chronic disease relapses; review cornea, tear film, lash loss and response rather than stopping all care after one improvement. 5. Stye (hordeolum) A hordeolum or stye is an acute, tender, localised infection/inflammation of an eyelid gland, usually staphylococcal. An external hordeolum involves a lash follicle/Zeis or Moll gland; an internal hordeolum

Introduction to Ophthalmology • Examination of the eye • Schiotz indentation tonometry Measuring Intraocular Pressure with a Schiotz Tonometer A Schiotz (Schiötz) tonometer is a contact indentation instrument that estimates intraocular pressure (IOP) by measuring how far a known plunger weight indents the anaesthetised cornea. It remains useful where slit-lamp applanation or electronic devices are unavailable, but it is technique-dependent and less accurate than modern reference methods. Students must understand both the procedure and the situations in which it should not be attempted. Safety first: Never perform contact tonometry on a suspected open globe, penetrating injury, leaking wound, severe unhealed corneal ulcer/abrasion or any eye where pressure could cause extrusion of contents. Shield and urgently refer. A Schiotz reading is an estimate, not a diagnosis of glaucoma. Learning objectives Define IOP and explain the principle of indentation tonometry. Identify the Schiotz tonometer parts, weights, test block and conversion chart. Check calibration, prepare the patient and perform the measurement safely. Know contraindications, infection-control requirements and common sources of error. Convert and document readings without inventing values or mixing conversion tables. Interpret abnormal results in context and arrange appropriate referral. 1. Intraocular pressure and clinical meaning IOP is the pressure within the globe, determined mainly by aqueous humour production and outflow, episcleral venous pressure, ocular rigidity and the balance of intraocular fluid. It helps maintain globe shape. A raised IOP can damage an at-risk optic nerve, but glaucoma is diagnosed through optic-nerve/retinal and visual-field changes, not pressure alone; normal-pressure glaucoma also exists. Concept Meaning Clinical application Raised IOP Pressure above the expected range for the method and patient. Confirm with a reliable method and assess optic disc/fields; urgent if acute symptoms. Ocular hypertension Raised IOP without definite glaucomatous damage. Risk assessment and monitoring, not automatic glaucoma treatment. Glaucoma Progressive optic-nerve/retinal nerve-fibre damage with characteristic field loss, often associated with IOP. Requires comprehensive ophthalmic assessment. Acute angle closure Rapid obstruction of aqueous outflow with painful pressure rise. Severe pain, halos, red eye, nausea/vomiting and visual loss are emergencies. Low IOP/hypotony Abnormally low globe pressure. May follow trauma, surgery, wound leak, inflammation or ciliary-body dysfunction. Many clinical references describe an approximate adult IOP range around 10–21 mmHg, but the patient’s cornea, posture, time of day, instrument and conversion table affect the result. Use the local laboratory/device reference and never interpret a number in isolation. 2. Principle of Schiotz indentation tonometry The patient lies supine with the cornea anaesthetised. A curved footplate rests gently on the central cornea. A standard plunger weight indents the cornea; the lower the IOP, the greater the indentation and the higher the scale reading. Higher IOP resists indentation, so the plunger moves less and the scale reading is lower. The scale reading is converted to an estimated mmHg using the conversion table supplied with that tonometer and plunger weight. The device does not directly sense pressure. Results are influenced by scleral rigidity, corneal thickness/biomechanics, ocular rigidity, patient posture, lid pressure, instrument alignment and the specific conversion table. It is best used by trained staff and confirmed with a modern method when the result is unexpected or clinically important. 3. Parts of the instrument Part Function Check before use Footplate Curved surface resting on the cornea. Clean, smooth, undamaged and free of residue. Plunger Moves vertically and indents the cornea. Moves freely without sticking; no bent shaft. Scale and pointer Indicate the indentation reading. Pointer moves smoothly and can return to zero. Standard weight Usually 5.5 g in standard teaching kits. Correct weight identified and securely fitted. Additional weights Commonly 7.5 g, 10 g and 15 g to extend the measurable range. Available, labelled and compatible with the instrument. Test block/artificial cornea Checks zero/calibration with the instrument upright or according to the manufacturer. Clean, stable and stored with the device. Conversion chart Converts scale plus weight to estimated IOP. Matches the instrument and table version; do not substitute a random table. Case/accessories Protects mechanism and stores weights/cleaning supplies. Complete, dry and labelled. 4. Indications Assessment of suspected glaucoma or ocular hypertension when a validated applanation/electronic method is unavailable. Monitoring a known patient when the same instrument and technique are used consistently. Assessment of pressure in selected painful red-eye presentations after open globe and corneal contraindications are excluded. Teaching indentation tonometry and community eye screening by trained personnel. In modern ophthalmic services, Goldmann applanation, calibrated handheld applanation, rebound or other validated methods may be preferred. A high, low or discordant Schiotz result should be confirmed. 5. Contraindications and precautions Do not perform or defer contact tonometry when… Reason/action Open globe or penetrating injury is suspected: irregular pupil, uveal prolapse, full-thickness wound, positive Seidel sign, severe high-velocity trauma. Pressure can extrude aqueous/vitreous and worsen injury. Rigid shield, no pressure and emergency referral. There is an unhealed corneal abrasion, ulcer, infiltrate, severe keratitis or active epithelial defect. Contact may worsen damage and spread infection; obtain specialist advice. There is active contagious conjunctivitis or corneal infection. Avoid cross-infection; use a different device/cover or defer. Follow decontamination policy. The patient cannot tolerate or is allergic to the topical anaesthetic. Do not force the procedure; use a validated non-contact/alternative method or refer. The instrument is damaged, uncalibrated, contaminated or missing its matching chart. Do not generate a false number; repair, calibrate or use an alternative. The patient cannot cooperate or remain still and no safe assistance is available. Do not restrain forcefully; seek experienced ophthalmic assessment. There is severe corneal irregularity, oedema, scar or unusual rigidity. Result may be unreliable; document limitation and confirm by another method. Before measuring a traumatised eye, complete a gentle visual/structural assessment. A normal-looking small wound does not exclude an open globe. 6. Equipment and preparation Schiotz tonometer with footplate, 5.5-g standard weight and additional weights. Manufacturer-supplied test block and matching conversion chart. Topical ophthalmic anaesthetic prescribed/authorised by the facility. Clean gloves, sterile gauze/cotton swabs and approved disinfectant compatible with the instrument. Clean tissue/saline and a rigid eye shield when trauma is possible. Patient record for scale reading, weight, converted IOP,

Introduction to Ophthalmology • Examination of the eye • External examination External Examination of the Eye: Lids, Cornea, Iris, Pupil and Lens A systematic external eye examination is a high-yield bedside skill. It begins before touching the patient: observe facial symmetry, eyelid position, redness, discharge, globe position and the patient’s ability to fixate. Then examine the lids, conjunctiva, cornea, anterior chamber, iris, pupil and lens with appropriate illumination and magnification. Always compare right and left eyes, and measure visual acuity early. Urgent warning: Do not manipulate a suspected open globe, remove an embedded foreign body, perform tonometry, force the eyelids open or apply a tight patch. A painful red eye with reduced vision, corneal opacity, abnormal pupil, proptosis, penetrating/chemical trauma or painful restricted movements requires urgent ophthalmology. Learning objectives Prepare a patient and perform a safe, structured external examination. Assess facial symmetry, lids, lashes, lacrimal system, conjunctiva, sclera, cornea, anterior chamber, iris, pupil and lens. Recognise normal findings and clinically important abnormalities. Use fluorescein, lid eversion, magnification and slit-lamp principles safely. Document findings and identify emergency referral criteria. 1. Preparation and sequence Introduce yourself, confirm identity, explain the examination and obtain consent. Ask about pain, photophobia, trauma, contact lenses, surgery, chemical exposure and visual change before manipulating the eye. Clean hands; use gloves if discharge, blood or chemical contamination is possible. Provide good diffuse light, then a focused oblique light and magnification if available. Examine from general to specific, right to left, without pressing the globe. Test distance acuity, pupils and movements before drops when clinically safe. Use fluorescein or lid eversion only when indicated and trained; avoid topical anaesthetic outside supervised examination. Sequence Look for General appearance Distress, photophobia, head posture, facial asymmetry, rash or trauma. Globe position/orbit Proptosis, enophthalmos, displacement, swelling, pulsation. Lids/lashes Ptosis, oedema, wounds, entropion, ectropion, trichiasis, vesicles, closure. Conjunctiva/sclera Injection pattern, chemosis, discharge, follicles/papillae, haemorrhage, jaundice. Cornea Clarity, shine, surface, foreign body, ulcer, scar, oedema and contour. Anterior chamber/iris Depth, cells/flare if slit lamp, hypopyon, hyphema, iris pattern and synechiae. Pupil Size, shape, equality, light/near response and RAPD. Lens/red reflex Transparency, cataract, dislocation and symmetry of red reflex. Motility Alignment, range, pain, diplopia and nystagmus. 2. General appearance and orbit Observe whether the patient keeps the eye closed, shields it from light, rubs it or has severe distress. Compare globe position from the front and above: proptosis is forward displacement; enophthalmos is posterior displacement; dystopia is abnormal vertical/horizontal position. Look for periorbital bruising, swelling, laceration, emphysema, crepitus, rash or vesicles. Assess facial symmetry and head posture. A compensatory tilt or chin position may indicate strabismus or ocular-motor palsy. Palpate orbital margins gently only when fracture/open globe is not suspected and avoid pressure on the globe. Orbital emergency clues Rapid proptosis, tense eyelids, reduced VA, RAPD, high IOP if safely measured, severe pain, ophthalmoplegia, colour desaturation or loss of light perception suggest orbital compartment syndrome. Fever, proptosis, painful restricted movements and systemic illness suggest orbital cellulitis. Both require immediate escalation. 3. Eyelids and eyelashes Structure/finding Normal appearance Abnormalities and significance Upper/lower lid Skin intact, margins appose the globe and blink is complete. Oedema, laceration, bruising, tumour, lagophthalmos or lid malposition. Ptosis Upper lid covers only a small superior corneal area. CN III palsy, Horner syndrome, myasthenia, muscle disease, aponeurotic or mechanical cause. Entropion Lid margin turns outward/neutral; lashes away from cornea. Inward turning causes trichiasis and corneal abrasion. Ectropion Punctum rests against globe. Outward turning causes tearing, exposure and conjunctival inflammation. Trichiasis Lashes point away from ocular surface. Lashes rub cornea, causing pain, photophobia and recurrent epithelial injury. Lagophthalmos Complete gentle closure. Exposure keratopathy in facial palsy, proptosis, sedation or unconsciousness. Lid margin Clean, smooth, no focal tenderness. Blepharitis, stye/hordeolum, chalazion, crusting, meibomian dysfunction. Canthi Medial/lateral angles intact. Medial canthal trauma may injure canaliculi; document and refer. Inspect the lid margin with the patient looking down and ask the patient to blink. Do not squeeze an acute lesion or manipulate a laceration until globe and lacrimal structures are assessed. 4. Conjunctiva and sclera Conjunctiva Inspect the palpebral conjunctiva by gently pulling down the lower lid. Upper-lid eversion may be needed for a subtarsal foreign body, but avoid it when open globe or severe trauma is suspected and seek trained assistance. Finding Description Possible cause Diffuse injection Superficial vessels over bulbar conjunctiva. Conjunctivitis, irritation, allergy or dry eye. Ciliary flush Deeper circumcorneal redness. Keratitis, uveitis or acute glaucoma. Chemosis Conjunctival oedema/ballooning. Allergy, infection, trauma or orbital congestion. Follicles Small pale elevations, often lower fornix. Viral/chlamydial infection or topical-drug reaction. Papillae Raised vascular cobblestone surface, often upper tarsal. Allergy, contact-lens reaction or chronic irritation. Subconjunctival haemorrhage Well-defined red patch. Spontaneous, trauma, strain, hypertension or anticoagulation. Foreign body Visible particle or focal inflammation. Requires safe removal/irrigation and corneal assessment. Sclera Normal sclera is white, although mild pigmentation or yellowing may be physiological or systemic. Diffuse yellowing suggests jaundice; focal pigmentation may be benign or pathological. Episcleritis is usually sectoral, superficial and milder; scleritis causes deep severe pain, tenderness and sometimes reduced vision. Do not press on a tender or traumatised globe. Deep violaceous redness with pain merits urgent ophthalmic evaluation. 5. Corneal examination Inspect the cornea with oblique light, magnification or slit lamp. Assess the lustre, transparency, contour, surface, epithelial integrity, vessels, foreign bodies and depth of any lesion. Corneal feature Normal Abnormal finding Clarity Transparent; iris detail visible. Haze, oedema, infiltrate, ulcer or scar. Surface/lustre Smooth, wet, reflective tear film. Punctate staining, abrasion, recurrent erosion or exposure changes. Contour Regular dome-shaped surface. Keratoconus, bulging, laceration or irregular foreign body. Vessels No central vessels. Neovascularisation from chronic hypoxia/inflammation. Arcus Peripheral grey-white lipid ring, often age-related. Early/prominent arcus may prompt systemic risk assessment; it should not explain acute pain. Infiltrate/ulcer Absent. White focal lesion, epithelial defect or stromal haze; urgent keratitis assessment. Fluorescein staining Fluorescein highlights epithelial defects under blue light. Instil a sterile strip/drop according to local protocol and avoid contamination. Diffuse punctate staining may reflect dry eye, exposure, toxicity or viral disease. A linear defect may indicate

Introduction to Ophthalmology • Examination of the eye • Visual assessment Assessment of Vision: Distance, Near and Visual Fields Visual assessment is the first objective examination in most eye complaints. It establishes a baseline, detects asymmetry and helps localise disease to the optical media, retina, optic nerve or visual pathways. Distance and near acuity answer different questions; visual-field assessment detects missing vision that a patient may not notice. Emergency principle: Measure and document vision early in every significant eye complaint. Sudden reduction, a new field defect, an afferent pupillary defect, visual loss after trauma/chemical exposure or a rapid change from baseline requires urgent escalation. Learning objectives Prepare a patient and test distance visual acuity accurately in each eye. Use correction, pinhole and low-vision notation appropriately. Assess near vision and recognise accommodation-related problems. Perform confrontation visual fields and understand their limitations. Explain Amsler-grid and formal perimetry principles. Document results clearly and identify emergency patterns. 1. Before testing Explain the purpose, reassure the patient and check language, literacy, hearing and ability to respond. Ensure good, even illumination without glare; place the correct chart at the prescribed distance. Ask about glasses/contact lenses and test with usual correction first when relevant. Test the right eye, then left eye, then both eyes; prevent peeking with an opaque occluder, not the patient’s fingers. Do not press on the covered eye. Record whether the patient can identify optotypes, count fingers, detect hand movement or perceive light. For acute disease, test before drops, patching or analgesia when clinically safe, and repeat after intervention if the situation changes. 2. Distance visual acuity Snellen and logMAR concepts Distance acuity is recorded as a fraction: the numerator is the testing distance and the denominator is the distance at which a standard eye can resolve the same optotype. A logMAR chart uses equal logarithmic steps and consistent letter spacing; it is often more precise for research and monitoring. Record Meaning Example Unaided/sc Without refractive correction. OD 6/24 sc. With correction/cc With the patient’s glasses or contact lenses. OS 6/9 cc. Pinhole Through a small aperture reducing defocus. OD 6/12 improving to 6/6 PH. Each eye Right and left separately. Do not report only binocular VA. Low vision Counts fingers, hand movement, light perception or no light perception. CF at 1 m; HM; PL positive; NPL. Procedure Seat the patient at the chart’s calibrated distance, commonly 6 m where available; use the chart’s specified distance if different. Ask the patient to keep both eyes open but occlude the non-tested eye completely without pressure. Start with a line the patient can reasonably see, then proceed to smaller lines until errors occur. Encourage but do not coach. Record the smallest line read according to local chart convention, including missed letters if the chart permits. Repeat with usual correction and pinhole if reduced and if no contraindication; pinhole does not diagnose the cause by itself. Test near vision separately, especially if the complaint is reading difficulty or distance vision is normal. Example documentation VA: OD 6/24 unaided, 6/12 with pinhole; OS 6/6 with habitual glasses; near N5 with correction. Pupils equal/reactive, no RAPD. This communicates asymmetry and a possible refractive component but does not exclude retinal or optic-nerve disease. 3. Pinhole interpretation Improvement suggests that refractive blur contributes to reduced acuity. No improvement may reflect corneal opacity, cataract, retinal/macular disease, optic-nerve dysfunction, amblyopia or poor technique. Pinhole is less useful in irregular astigmatism, dense media opacity or very low vision. A patient with sudden loss, pain, field defect or RAPD needs urgent evaluation regardless of pinhole response. 4. Measuring very poor vision Level How to test Documentation Counting fingers (CF) Show fingers at a measured distance, moving closer if needed. CF at 2 m, CF at 1 m or CF close to face. Hand movements (HM) Move hand against a contrasting background. HM positive/negative; test direction if relevant. Light perception (LP/PL) Use a light from different quadrants; ask if seen and where. PL positive with/without projection. No light perception No response to appropriate light stimulus. NPL; confirm technique and both eyes. Do not convert CF, HM or PL into a falsely precise Snellen fraction. Record the method, distance, illumination and patient cooperation. 5. Near visual acuity Near acuity tests the ability to resolve print at a specified distance, commonly around 35–40 cm, using a near card with standard notation such as N notation, Jaeger or equivalent. The patient should use near correction if normally worn. Illuminate the card evenly without glare. Hold it at the specified distance; do not let the patient bring it closer without recording the change. Test each eye separately and then both eyes if useful. Record the smallest line read and the correction used. Reduced near vision with normal distance vision Possible explanations Age-related difficulty Presbyopia or reduced accommodative reserve. Eye strain/fluctuation Dry eye, uncorrected astigmatism, convergence/accommodation disorder. Central distortion Macular disease; ask about metamorphopsia and test each eye. Neurological difficulty reading Field loss, neglect, visual agnosia or cognitive/attention problem. 6. Visual-field assessment The visual field is the total area visible while the patient fixates steadily. Testing each eye separately identifies monocular defects; testing both eyes helps understand functional impact. A patient may not notice a field defect because the brain fills in missing information. Confrontation fields Sit facing the patient at approximately the same eye level and ask the patient to fixate on your nose or a central target. Test one eye at a time by having the patient cover the opposite eye without pressure; cover your corresponding eye. Bring a finger or small target from the periphery toward the centre in each quadrant, comparing with your own field. Ask when the patient first sees it and whether it is equally bright. Repeat with a red target when a subtle defect is suspected. Map a defect by moving the target along different meridians; document central versus peripheral and the side/quadrant involved. Finding Possible localisation Monocular central scotoma Macula or optic nerve. Monocular peripheral loss Retina, optic nerve or advanced glaucoma.

Introduction to Ophthalmology • Ophthalmic symptomatology • Secretions and appearance Abnormal Ocular Secretions and Appearance: Watery, Purulent Discharge and Redness Watery eyes, sticky or purulent discharge, swelling and redness are common reasons for seeking care. They may reflect a benign surface disorder, but the same appearance can occur in corneal ulcer, uveitis, acute glaucoma, orbital cellulitis, chemical injury or neonatal infection. The clinician must describe the secretion and vascular pattern, measure vision and search for pain, photophobia and systemic danger signs. Urgent warning: Redness with reduced vision, severe pain, photophobia, corneal opacity, hypopyon, high-risk trauma/chemical exposure, contact-lens use, proptosis, fever, painful eye movements or a fixed/irregular pupil needs same-day ophthalmic assessment. Neonatal profuse purulent discharge is an emergency. Learning objectives Distinguish watery, mucoid, mucopurulent and purulent ocular secretions. Describe conjunctival, ciliary, episcleral and diffuse redness accurately. Differentiate common conjunctivitis from keratitis, uveitis, acute glaucoma, trauma and orbital infection. Take a focused history, perform an initial eye examination and identify referral red flags. Provide safe hygiene, infection-control, irrigation and referral advice. 1. Describe what is visible Finding Useful description Possible meaning Watery/serous tears Clear, thin, continuous or intermittent; one or both eyes. Viral infection, allergy, irritation, corneal abrasion, obstruction or reflex tearing from dry eye. Mucoid/stringy White/clear mucus, ropy strands, often with itching. Allergy, dry eye or chronic surface disease. Mucopurulent Sticky yellow/green discharge that reforms after cleaning. Bacterial conjunctivitis or other infection; severity and vision determine urgency. Profuse purulent Copious thick pus, eyelids stuck, rapid reaccumulation. Hyperacute bacterial infection such as gonococcal conjunctivitis; emergency due to corneal melt/perforation. Crusting Dried discharge on lashes or lid margins. Blepharitis or conjunctivitis; assess chronicity and recurrent lesions. Diffuse conjunctival injection Generalised superficial redness that blanches with pressure. Conjunctivitis, irritation, allergy or dry eye. Ciliary flush Deep violaceous ring around the limbus. Keratitis, anterior uveitis or acute glaucoma until assessed. Subconjunctival haemorrhage Well-demarcated bright-red patch beneath conjunctiva. Often benign, but trauma, bleeding risk or recurrence require assessment. Chemosis Oedematous, ballooned conjunctiva. Allergy, infection, trauma, inflammation or orbital venous congestion. Corneal opacity/white spot Loss of transparency, infiltrate, scar or oedema. Corneal ulcer, keratitis, oedema or injury; vision-threatening if central/infectious. 2. Focused history Onset/course: sudden, gradual, recurrent, progressive, after waking or following exposure. Laterality/spread: one eye then the other, bilateral from onset, household/school outbreak. Discharge: clear, mucous, yellow/green, bloody, amount, frequency and whether it reforms quickly. Vision: blur, reduced acuity, glare, halos, flashes, floaters or field loss. Pain/photophobia: surface irritation versus severe/deep pain and light intolerance. Trauma/exposure: chemical, dust, high-velocity object, welding, swimming, cosmetics or foreign body. Contact lenses: overnight wear, hygiene, water exposure, replacement and current use. Systemic context: fever, respiratory illness, rash, sexually transmitted infection risk, immunosuppression, autoimmune disease. Neonatal/pregnancy history: age at onset, delivery complications, maternal infection and prophylaxis. Past eye disease: glaucoma, uveitis, herpetic eye disease, surgery, injections or one-eyed status. 3. Initial examination Examination What to document Reason Visual acuity Each eye, correction/pinhole, CF/HM/PL if very poor. Reduced VA is a red flag in a red eye. Pupils Size, shape, reactivity, RAPD. Optic-nerve/retinal disease or acute glaucoma. Lids/lashes Swelling, crusting, vesicles, entropion, trichiasis and closure. Blepharitis, herpes, exposure and cellulitis clues. Conjunctiva Pattern, blanching, chemosis, haemorrhage, follicles/papillae where trained. Helps separate superficial from deep inflammation. Cornea/anterior chamber Clarity, epithelial defect, infiltrate, hypopyon, depth and cells/flare. Keratitis, ulcer, uveitis and glaucoma can threaten sight. Motility/orbit Proptosis, movement restriction/pain and diplopia. Orbital cellulitis or compartment pathology. Fluorescein/IOP Only if safe and equipment/training are available. Detects epithelial damage; pressure helps selected cases but is unsafe with open globe. 4. Watery eyes (epiphora) Mechanism Examples Clues Reflex overproduction Corneal abrasion, foreign body, keratitis, dry eye, allergy, smoke/wind. Tearing accompanies irritation, pain, itching or blinking. Drainage obstruction Punctal stenosis, canalicular disease, nasolacrimal duct obstruction, infection. Overflowing tears, often unilateral; discharge/medial canthal swelling may occur. Lid malposition Entropion, ectropion, laxity, facial-nerve palsy. Abnormal punctal position or exposed ocular surface. Inflammation/infection Viral conjunctivitis, uveitis, keratitis. Redness, photophobia or visual reduction changes urgency. Dry eye can paradoxically cause tearing: an unstable tear film stimulates corneal nerves and produces reflex aqueous tears that rapidly overflow because the underlying surface remains abnormal. 5. Purulent and mucopurulent discharge Common bacterial conjunctivitis Redness, gritty discomfort, mucopurulent discharge and eyelids stuck on waking; vision should remain near baseline after discharge is cleared. Usually superficial, but contact-lens wear, pain, photophobia, corneal opacity or reduced VA suggests keratitis and requires urgent review. Hand hygiene, individual towels and avoidance of sharing cosmetics reduce spread. Antibiotic treatment depends on clinical assessment and local protocol. Hyperacute purulent conjunctivitis Copious rapidly recurring pus, severe chemosis, pain or corneal involvement should be treated as an emergency. Gonococcal infection can invade intact epithelium and cause corneal ulceration/perforation. Obtain urgent ophthalmic and sexual-health/infectious-disease assessment; collect appropriate specimens before treatment when this does not delay care, and arrange partner/public-health management. Neonatal purulent discharge Profuse discharge in a newborn may be caused by gonococcal or chlamydial infection and can rapidly damage the cornea. Urgent paediatric/ophthalmic evaluation and systemic treatment are required; do not rely on routine topical drops alone. 6. Red eye: pattern matters Pattern Likely categories Features that demand escalation Diffuse superficial injection Viral/allergic/bacterial conjunctivitis, irritation, dry eye. Reduced VA, severe pain, photophobia, corneal opacity, contact lens, neonatal age. Marked itching and chemosis Allergic conjunctivitis. Airway/facial swelling, severe unilateral disease or visual change. Perilimbal/ciliary flush Keratitis, uveitis, acute glaucoma. Any pain, photophobia, reduced VA, irregular/fixed pupil or hypopyon. Sectoral deep redness Episcleritis or scleritis. Deep severe pain, tenderness, autoimmune symptoms or visual loss. Subconjunctival haemorrhage Spontaneous, trauma, cough/strain, hypertension or anticoagulation. Penetrating trauma, recurrent bleeding, pain or reduced vision. Red swollen lids with fever Preseptal/orbital cellulitis. Proptosis, restricted painful movements, RAPD, reduced VA or systemic toxicity. 7. Differential diagnosis of red eye Condition Pain Photophobia Vision Pupil/cornea Urgency Viral conjunctivitis Mild gritty. Mild. Usually preserved. Clear cornea; watery discharge. Routine unless atypical/severe. Allergic conjunctivitis Itch/burning. Usually mild. Preserved. Chemosis/stringy mucus. Urgent if severe swelling/airway symptoms. Bacterial conjunctivitis Mild-moderate. Usually mild. Preserved after cleaning. Mucopurulent; cornea usually clear. Urgent if hyperacute or corneal involvement.

Introduction to Ophthalmology • Ophthalmic symptomatology • Abnormal sensations Abnormal Ocular Sensations: Pain, Dryness, Itching and Foreign-Body Sensation Ocular sensation is generated by a richly innervated ocular surface and by deeper intraocular, orbital and neural structures. Pain, dryness, itching, burning and the feeling that something is in the eye are common complaints, but their urgency varies widely. A superficial irritant may be minor; a corneal ulcer, acute glaucoma, orbital infection, chemical injury or neurological process can threaten sight and life. Emergency warning: Severe or deep eye pain, pain with reduced vision, photophobia, corneal opacity, contact-lens use, chemical/penetrating trauma, proptosis, fever, painful eye movements, fixed pupil, severe headache/vomiting or pain after surgery/injection requires urgent ophthalmic assessment. Learning objectives Define pain, dryness, itching, burning, photophobia, foreign-body sensation and pain on movement. Use history and examination to separate ocular-surface, intraocular, orbital, neurological and referred causes. Recognise sight-threatening causes that can initially resemble “conjunctivitis” or irritation. Provide safe first aid, including irrigation and foreign-body precautions. Explain hospital assessment, treatment principles, prevention and patient education. 1. Understanding ocular sensation Sensation Patient’s words Possible anatomical source Pain Sharp, stabbing, aching, boring, throbbing or severe. Corneal nerves, uvea, sclera, orbit, optic nerve, trigeminal pathways or referred structures. Burning/stinging “It burns,” “soap in my eye,” “hot or irritated.” Tear-film/epithelial irritation, chemical exposure, allergy or topical medication. Itching “I want to rub it.” Conjunctival allergy, lid-margin disease or dermatitis. Dryness/grittiness Sand, dust, tired or sticky eyes. Tear-film instability, aqueous deficiency, meibomian disease, exposure or medication effect. Foreign-body sensation Something is stuck or scratching with blinking. Corneal abrasion, subtarsal foreign body, conjunctival lesion, trichiasis or contact-lens complication. Photophobia Light is painful or intolerable. Corneal/uveal inflammation, migraine, meningism or severe surface injury. Pain on movement Deep pain when looking around. Optic neuritis, orbital inflammation, cellulitis, muscle or orbital trauma. 2. Focused history Onset: exact time, sudden/gradual, exposure-related, recurrent or progressive. Site and depth: surface scratch versus deep ache behind the eye; unilateral or bilateral. Quality/severity: burning, itching, gritty, sharp, boring, pulsating; use a pain scale and functional impact. Triggers: blinking, eye movement, light, reading, screens, wind, smoke, contact lenses or a chemical. Associated visual symptoms: blur, reduced acuity, halos, flashes, floaters, field loss, diplopia or colour change. Inflammatory/systemic features: redness, discharge, fever, headache, nausea/vomiting, rash, joint pain, autoimmune disease or immunosuppression. Trauma and procedure: grinding/welding, high-velocity object, surgery, injection, foreign body, rubbing or recent anaesthesia. Contact lens history: overnight wear, water exposure, poor cleaning, replacement and current use. Medication history: drops, preservatives, steroids, glaucoma medicines, isotretinoin, antihistamines, anticholinergics and systemic drugs causing dryness. Past eye history: glaucoma, uveitis, corneal disease, herpes, surgery, one-eyed status or recurrent erosions. 3. Initial examination and safety Step Key points Danger if missed Vital signs/systemic assessment Temperature, blood pressure, mental status, glucose when indicated. Sepsis, severe hypertension, meningitis or metabolic disease. Visual acuity Each eye separately with correction and pinhole if appropriate. Reduced VA changes a “simple irritation” into an urgent problem. Pupils/RAPD Size, shape, reactivity and swinging-light response. Optic-nerve/retinal disease, acute glaucoma or neurological pathology. External exam Lids, lashes, conjunctiva, ciliary flush, cornea, proptosis, discharge and trauma. Ulcer, open globe, cellulitis, severe inflammation. Motility Movement limitation or pain, diplopia and nystagmus. Orbital cellulitis, optic neuritis, fracture or cranial-nerve palsy. Fluorescein/slit lamp For epithelial defect, infiltrate, foreign body, cells/flare or Seidel leak when safe. Corneal ulcer, penetrating injury or intraocular inflammation. IOP Only after open globe is excluded and trained staff/equipment are available. Pressure on an open globe can worsen injury. 4. Ocular pain Cause group Examples Typical clues Corneal/surface Abrasion, keratitis, ulcer, recurrent erosion, foreign body, chemical injury. Severe pain, photophobia, tearing, blink-related discomfort, fluorescein defect or opacity. Anterior intraocular Anterior uveitis/iritis, acute angle-closure glaucoma. Ciliary flush, photophobia, blurred vision, small/irregular or mid-dilated pupil, cells/flare or high IOP. Deep ocular coat Scleritis, posterior uveitis. Deep boring pain, tenderness, pain with movement or autoimmune disease. Orbital Orbital cellulitis, abscess, haemorrhage, fracture, tumour or thyroid eye disease. Proptosis, restricted/painful movement, fever, diplopia or optic-nerve signs. Optic nerve Optic neuritis, ischaemic or compressive optic neuropathy. Reduced colour/central vision, RAPD, pain on movement or field loss. Neurological/referred Migraine, trigeminal neuralgia, cluster headache, sinus disease, meningitis. Headache pattern, neurological or systemic signs; ocular examination may be normal. Corneal pain is often intense because the epithelium is supplied by trigeminal sensory fibres. Deep pain with reduced vision, a quiet-looking eye and RAPD is not reassuring; optic-nerve or orbital disease may be hidden behind the globe. 5. Dryness, burning and grittiness Dry-eye disease occurs when tear-film homeostasis fails. The problem may be insufficient aqueous production, excessive evaporation, poor lipid secretion, abnormal mucin/surface interaction, inflammation or exposure. Mechanism Examples Associated clues Aqueous deficiency Sjögren syndrome, lacrimal-gland disease, age-related reduction, systemic medicines. Persistent dryness, foreign-body sensation, reduced tear meniscus. Evaporative loss Meibomian-gland dysfunction, blepharitis, wind, smoke, screens and incomplete blinking. Fluctuating blur, lid crusting, oily tear film or worse late in the day. Exposure Lagophthalmos, facial-nerve palsy, proptosis, intensive-care sedation. Inferior staining, nocturnal symptoms and risk of exposure keratopathy. Surface toxicity/inflammation Preserved drops, allergy, chronic topical medicines, chemical irritation. Burning after drops, redness and worsening with frequent self-medication. Safe management principles Remove smoke, dust, wind and avoid prolonged uninterrupted screen viewing; encourage regular blinking and breaks. Use preservative-free lubricants when frequent treatment is required and follow local product guidance. Treat lid-margin disease with warm compresses and gentle hygiene when appropriate; avoid squeezing lesions. Assess exposure, facial weakness, contact lenses, autoimmune symptoms and medication causes. Refer urgently when pain, photophobia, reduced vision, corneal opacity or contact-lens use is present. 6. Itching and rubbing Itching strongly suggests ocular allergy, but rubbing can worsen epithelial injury, spread infection and contribute to keratoconus in susceptible people. Allergic conjunctivitis often causes bilateral itching, watering, chemosis and stringy mucus; it should not cause severe pain or marked visual loss. Ask about seasonal exposure, dust, cosmetics, pets, atopy, asthma, eczema and new medicines. Use cool compresses, allergen reduction and clinician-directed topical anti-allergic therapy when indicated. Avoid sharing towels or drops; wash hands and avoid rubbing. Severe unilateral pain, photophobia, reduced

Introduction to Ophthalmology • Ophthalmic symptomatology • Abnormal vision Abnormal Vision: Blurred Vision, Peripheral Field Loss, Glare and Floaters “Abnormal vision” is a symptom group, not a diagnosis. A patient may describe blur, dimness, missing areas, glare, halos, flashes, floaters, distortion, double vision or complete loss. The clinician’s first task is to protect sight and identify time-critical disease, then localise the problem to the optical media, retina, optic nerve, visual pathway, orbit or brain. Urgent warning: Sudden visual loss, a new curtain or field defect, new flashes with many floaters, painful red eye with reduced vision, visual loss after trauma or chemical exposure, acute diplopia with neurological signs, or proptosis with fever requires same-day emergency assessment. Do not reassure a patient simply because the eye is not red or painful. Learning objectives Define and distinguish blurred vision, reduced peripheral vision, glare/halos, floaters, flashes, distortion, diplopia and visual loss. Take a focused history that separates ocular, neurological, systemic, medication and functional causes. Recognise red flags for retinal detachment, vascular occlusion, acute glaucoma, optic neuropathy, orbital disease and stroke. Perform a safe first assessment: visual acuity, pupils, fields, eye movements and external examination. Provide first aid and referral while avoiding harmful delays, pressure or inappropriate eye drops. Explain hospital investigations, treatment principles, follow-up and prevention. 1. What does the patient mean by “I cannot see properly”? Patient description Clinical term Clarifying question “Everything is out of focus.” Blurred vision. Is it near, distance, one eye or both? Does pinhole or blinking help? “I cannot see to the side.” Peripheral field loss/scotoma. Is the missing area fixed, moving, one side of both eyes or one eye? “Headlights spread and hurt.” Glare/light scatter. Is it worse at night, in bright light, with cataract, dry eye or contact lenses? “Cobwebs or black dots move with my eye.” Floaters/entoptic shadows. New or longstanding? Flashes? Curtain? Trauma or myopia? “Flashes of lightning.” Photopsias. New? Peripheral? With floaters or field loss? “A curtain came down.” Acute field loss or amaurosis. Which eye, how long, complete or partial, and did it recover? “Straight lines are bent.” Metamorphopsia. Central distortion? Test each eye and consider macular disease. “I see two.” Diplopia. Does it disappear when either eye is covered? “The world went dark.” Severe visual loss/amaurosis. Exact onset, last-known-well time and associated neurological symptoms. 2. Focused history Onset and time: exact time, sudden versus gradual, transient versus persistent, first episode or recurrent. Laterality: right, left or both. Ask the patient to cover each eye separately during symptoms. Pattern: central, peripheral, general dimness, patch/scotoma, distortion, movement-related or position-related. Severity and function: reading, faces, walking, driving, colour, light perception and occupational tasks. Pain and inflammation: pain, pain on eye movement, photophobia, redness, discharge, headache, nausea/vomiting. Retinal symptoms: flashes, shower of floaters, curtain, field defect, night blindness. Neurological symptoms: weakness, numbness, speech difficulty, imbalance, altered consciousness or severe headache. Trauma/exposure: blunt or penetrating injury, grinding/welding, chemical splash, foreign body, recent surgery or injection. Risk factors: myopia, diabetes, hypertension, sickle-cell disease, vascular disease, migraine, glaucoma, autoimmune disease, infection, pregnancy, smoking and immunosuppression. Medicines: steroids, anticholinergics, glaucoma drops, hydroxychloroquine, ethambutol, topiramate, anticoagulants and drugs causing sedation or visual disturbance. Contact lenses: type, overnight wear, hygiene, water exposure, replacement schedule and current use. Family and eye history: retinal detachment, glaucoma, macular disease, previous surgery, amblyopia or one-eyed status. 3. Immediate assessment at first contact Assessment How to do it safely Why it matters Airway, breathing, circulation and disability Stabilise life threats first; check glucose when altered or neurological. Stroke, hypoglycaemia, seizure and trauma can present with visual symptoms. Visual acuity Test each eye separately with usual correction; record chart and distance, then pinhole if appropriate. Objective baseline and major triage discriminator. Pupils Size, shape, equality, direct/consensual responses and swinging-light test. RAPD suggests optic-nerve or severe retinal dysfunction. Visual fields Confrontation by eye, noting central/peripheral defects. Identifies retinal, optic-pathway and neurological patterns. Eye movements Versions/ductions, pain, nystagmus, diplopia and restriction. Localises cranial-nerve, muscle, orbit or brainstem disease. External eye Lids, conjunctiva, cornea clarity, pupil, proptosis, trauma and discharge. Red eye, open globe, orbital disease and infection can be visible. IOP/fluorescein Only when open-globe injury is not suspected and trained equipment/protocol is available. Helps identify glaucoma or epithelial injury without causing harm. Never press on a suspected open globe. Do not force the eyelids open, remove an embedded object, patch tightly, perform tonometry or instil drops before specialist advice. Use a rigid shield, avoid food if anaesthesia may be needed and arrange urgent ophthalmology. 4. Blurred vision Blur may originate anywhere from tear film to visual cortex. The pattern and associated findings are more informative than the word “blur.” Category Examples Clues Optical/refractive Myopia, hyperopia, astigmatism, presbyopia. Gradual, often painless; improves with pinhole or correct lenses; no RAPD. Ocular surface/cornea Dry eye, abrasion, keratitis, ulcer, oedema, scar. Fluctuation, pain, photophobia, foreign-body sensation, staining or opacity. Lens Cataract, lens displacement, postoperative change. Glare, gradual painless decline, reduced red reflex; trauma may be acute. Retina/macula Diabetic oedema, macular degeneration, detachment, haemorrhage. Distortion, central scotoma, floaters, flashes or field loss. Optic nerve Optic neuritis, ischaemic optic neuropathy, compression. Colour desaturation, RAPD, central field loss, pain on movement or sudden loss. Neurological Stroke, occipital lesion, migraine aura, seizure. Field pattern, neurological signs, transient/recurrent features. Systemic/metabolic Hypoglycaemia, severe hypertension, anaemia, toxic medication effects. Systemic symptoms or bilateral fluctuation; still assess the eyes. Functional/non-organic Visual symptoms without an anatomical explanation. Diagnosis of exclusion after respectful examination; never assume malingering. 5. Reduced peripheral vision and visual-field defects Peripheral vision is the ability to detect objects outside the point of fixation. Field loss may be retinal, optic-nerve, chiasmal, retrochiasmal or cortical. Patients may describe bumping into objects, missing people approaching from one side, difficulty driving or a “tunnel.” Pattern Possible localisation Examples/next step Monocular peripheral defect Retina or optic nerve before the chiasm. Retinal detachment, glaucoma, optic neuropathy; test each eye separately. Bitemporal hemianopia Optic chiasm, especially crossing nasal fibres. Sellar/parasellar mass; urgent neurological and ophthalmic evaluation. Homonymous hemianopia Optic tract, radiations or occipital cortex