Ophthalmology

Chronic inflammation of the eyelid margins. Anterior blepharitis affects the lash bases (staphylococcal or seborrhoeic); posterior blepharitis is meibomian gland dysfunction (MGD), strongly linked to rosacea and seborrhoeic dermatitis. Bilateral, relapsing-remitting gritty sore eyes — a clinical diagnosis managed conservatively, NOT with antibiotics first-line.

An acute, painful, localised staphylococcal infection of an eyelid gland. External hordeolum (common stye) points at the lash line (gland of Zeis/Moll); internal hordeolum is an infected meibomian gland pointing on the inner lid. Self-limiting — warm compresses, NOT antibiotics.

A chronic, painless granulomatous swelling from a blocked meibomian gland — a sterile lipogranuloma, not an infection. Follows MGD/blepharitis. Most resolve with warm compresses; persistent ones may need incision and curettage.

Outward turning of the (usually lower) eyelid margin away from the globe, most often involutional (age-related lid laxity). Exposes the palpebral conjunctiva, causing watering (epiphora), exposure keratopathy and irritation.

Inward turning of the (usually lower) eyelid margin so the lashes rub the cornea/conjunctiva (trichiasis), causing pain, foreign-body sensation and a risk of corneal abrasion/ulcer. Usually involutional; cicatricial forms follow scarring (e.g. trachoma).

Acute infective conjunctivitis with purulent discharge, usually self-limiting (5–7 days). Most need no antibiotic; topical chloramphenicol if severe or rapid resolution required. Hyperacute purulent conjunctivitis in a sexually active adult/neonate raises gonococcal/chlamydial causes (ophthalmia neonatorum).

Highly contagious adenoviral conjunctivitis, usually following a URTI. Watery discharge, follicular reaction and a tender preauricular node. Self-limiting over 1–2 weeks; no antibiotic. The key exception is herpetic (HSV) infection, which must not be steroided or missed.

IgE-mediated conjunctival hypersensitivity. Bilateral itch (the cardinal symptom) with watering, chemosis and stringy mucus, on an atopic background. Treated with allergen avoidance, antihistamine/mast-cell-stabiliser drops. Vernal and atopic keratoconjunctivitis are severe, sight-threatening variants.

A flat, painless, well-demarcated patch of blood under the conjunctiva from a ruptured vessel. Benign and self-limiting; the role of the clinician is to reassure and to check for the few meaningful associations (hypertension, anticoagulation, trauma; bilateral/recurrent → bleeding tendency).

A wing-shaped fibrovascular growth of conjunctiva extending onto the nasal cornea, driven by chronic UV/wind/dust exposure ('surfer's/farmer's eye'). Usually cosmetic/irritative; surgery if it threatens the visual axis or causes astigmatism.

Keratoconjunctivitis sicca — a multifactorial disease of tear-film instability causing ocular surface inflammation. Evaporative (MGD-related) is commonest; aqueous-deficient forms include Sjögren syndrome. Diagnosis and primary management are symptom-led; refer for serious causes or non-response.

Infection of the lacrimal sac secondary to nasolacrimal duct obstruction. Presents with a painful, red, tender swelling at the medial canthus (below the medial canthal tendon) with epiphora. Acute cases need oral antibiotics; recurrent cases need dacryocystorhinostomy (DCR).

A traumatic epithelial defect of the cornea (fingernail, branch, foreign body, contact lens). Acutely painful with watering and photophobia; stains green with fluorescein. Heals quickly; the priorities are excluding a penetrating injury/foreign body and avoiding infection (especially in lens wearers).

A sight-threatening infection of the corneal stroma (corneal ulcer). Strongly associated with contact-lens wear (especially overnight); Pseudomonas causes rapid, aggressive ulcers. Presents as a painful red eye with a white corneal infiltrate ± hypopyon. An ophthalmic emergency — scrape, intensive topical antibiotics, NO steroids/lenses.

Corneal infection by herpes simplex virus, classically an epithelial dendritic ulcer (branching, terminal end-bulbs) that stains with fluorescein, often recurrent and unilateral with reduced corneal sensation. Treated with topical/oral antivirals; topical steroids alone are dangerous and can cause a geographic ulcer.

A protozoal corneal infection, classically in contact-lens wearers exposed to water (showering/swimming in lenses, tap-water rinsing). Causes severe pain out of proportion to signs, a ring-shaped stromal infiltrate and perineural involvement (radial keratoneuritis). Hard to diagnose and treat — vision-threatening.

Progressive non-inflammatory thinning and conical protrusion of the cornea, presenting in teens/twenties with worsening irregular (myopic) astigmatism. Associated with atopy/eye-rubbing, Down and connective-tissue syndromes. Managed with rigid/scleral lenses and corneal cross-linking to halt progression.

Inflammation of the anterior uveal tract (iris ± ciliary body). Acute anterior uveitis presents with a painful, photophobic red eye with reduced vision; strongly associated with HLA-B27 disease (ankylosing spondylitis, IBD, reactive arthritis, psoriatic arthritis). Managed by ophthalmology with topical steroids and cycloplegia.

A painful, potentially sight-threatening inflammation of the sclera, frequently associated with systemic disease (rheumatoid arthritis, granulomatosis with polyangiitis, other vasculitides). Severe boring pain that wakes the patient, deep violaceous injection that does NOT blanch with topical phenylephrine. Needs systemic anti-inflammatory treatment.

Benign, self-limiting inflammation of the episclera. A localised red eye with mild or no pain and normal vision; the redness blanches with topical phenylephrine (superficial vessels). Reassurance ± lubricants/NSAID; the key skill is distinguishing it from sight-threatening scleritis.

A sudden rise in intraocular pressure when the iris blocks the trabecular drainage angle (pupillary block). An ophthalmic emergency presenting with a painful red eye, haloes, a hazy cornea and a fixed mid-dilated oval pupil, often with nausea and vomiting. Risk factors: hypermetropia, age, female sex, dilation (dark rooms, mydriatics, anticholinergics).

A chronic, progressive optic neuropathy with an open drainage angle, characteristically asymptomatic until advanced. Defined by optic-disc cupping and arcuate visual-field loss, usually with raised IOP. Detected on routine optometry. NICE (2022): first-line treatment is now 360° selective laser trabeculoplasty (SLT) for those with IOP ≥24 mmHg needing treatment.

Opacification of the crystalline lens causing gradual, painless visual loss with glare and reduced contrast. Mostly age-related; secondary causes include diabetes, corticosteroids, uveitis, trauma and congenital infection. Definitive treatment is day-case phacoemulsification with intraocular lens implant; NICE: do not ration surgery by visual acuity.

Lens opacity present at/near birth — a key cause of an absent red reflex / leukocoria found on the newborn and 6-week checks. Causes include genetic (often autosomal dominant), intrauterine infection (congenital rubella, other TORCH), and metabolic disease (galactosaemia). Needs urgent referral: early surgery prevents irreversible deprivation amblyopia.

Sudden, painless, profound monocular visual loss from occlusion of the central retinal artery — effectively a retinal stroke. Causes: carotid/cardiac embolism, and crucially giant cell arteritis. Fundus shows a pale retina with a cherry-red spot and an RAPD. Time-critical, with a poor prognosis; treat as a stroke/TIA equivalent and exclude GCA.

Occlusion of the central retinal vein causing sudden, painless, variable monocular visual loss. The fundus shows widespread flame and dot-blot haemorrhages, dilated tortuous veins, cotton-wool spots and disc/macular oedema ('blood and thunder' / stormy-sunset fundus). Risk factors: hypertension, diabetes, hyperviscosity, glaucoma. Treated with anti-VEGF for macular oedema; watch for neovascular complications.

Separation of the neurosensory retina from the underlying retinal pigment epithelium, most often rhegmatogenous (a retinal tear lets fluid track underneath). Presents with new flashes, a shower of floaters and a progressing 'curtain' over the visual field. A surgical emergency if the macula is still attached ('macula-on'). Risk factors: myopia, prior cataract surgery, trauma, posterior vitreous detachment.

Age-related separation of the vitreous gel from the retinal surface — very common and usually benign. Causes acute flashes and floaters (including a ring floater, the Weiss ring). The essential task is to exclude an associated retinal tear/detachment, since PVD can tear the retina as it separates.

Bleeding into the vitreous cavity, causing sudden painless floaters, haze or visual loss with loss of the red reflex. The commonest cause is proliferative diabetic retinopathy (bleeding from new vessels); also retinal tear/PVD, retinal vein occlusion and trauma. Needs referral to find and treat the source.

Microvascular retinal damage from chronic hyperglycaemia — the leading cause of blindness in the working-age population. Graded non-proliferative (microaneurysms, dot-blot haemorrhages, exudates, cotton-wool spots) → proliferative (retinal neovascularisation, risking vitreous haemorrhage and tractional detachment). Diabetic maculopathy (macular oedema) is the main cause of vision loss. Annual screening; treat with laser/anti-VEGF and glycaemic/BP control.

Retinal microvascular changes caused by hypertension, graded (Keith-Wagener-Barker) from arteriolar narrowing through AV nipping and flame haemorrhages/cotton-wool spots to papilloedema (malignant/accelerated hypertension). Usually asymptomatic; finding it should prompt BP assessment and, with papilloedema, urgent treatment.

Degeneration of the central macula and the leading cause of central visual loss in older people. Dry (atrophic) AMD is gradual, with drusen and geographic atrophy; wet (neovascular) AMD involves choroidal neovascularisation with rapid central distortion and is treated with intravitreal anti-VEGF. Central vision is lost; peripheral/navigational vision is preserved.

An inherited (often autosomal-recessive/dominant/X-linked) progressive degeneration of photoreceptors — rods first. Presents with childhood/young-adult night blindness and progressive peripheral (tunnel) field loss. Classic fundus: bone-spicule pigmentation, attenuated vessels and a waxy pale disc. May be syndromic (Usher = + deafness; Bardet-Biedl).

Inflammatory demyelination of the optic nerve, most often the first or a relapsing manifestation of multiple sclerosis. Subacute monocular visual loss over hours-days with pain on eye movement, dyschromatopsia (red desaturation) and a relative afferent pupillary defect. Treated with IV methylprednisolone (speeds recovery); MRI assesses MS risk.

Optic-disc swelling caused by raised intracranial pressure — by definition BILATERAL. It is a sign, not a diagnosis: the task is to find and treat the cause (space-occupying lesion, idiopathic intracranial hypertension, venous sinus thrombosis, meningitis, malignant hypertension). Vision is preserved early but chronic papilloedema causes progressive field loss.

Infarction of the anterior optic nerve head causing sudden, painless, often altitudinal visual loss with a swollen disc. Arteritic AION is due to giant cell arteritis (an emergency — bilateral blindness risk); non-arteritic AION occurs in small 'disc-at-risk' eyes with vascular risk factors. Amaurosis fugax (transient monocular 'curtain') is a TIA-equivalent warning of carotid/cardiac embolism or GCA.

Vivid, complex visual hallucinations (people, animals, patterns) experienced by people with significant visual loss (e.g. AMD, glaucoma, diabetic retinopathy) who have INTACT insight and no psychiatric or cognitive disorder. It is a release phenomenon of the deprived visual cortex — benign and reassuring to recognise, not a psychosis.

Strabismus (squint) is misalignment of the visual axes. Concomitant strabismus (constant angle in all directions, usually childhood esotropia) is commonest; incomitant/paralytic strabismus follows a cranial-nerve palsy. Amblyopia is reduced vision in a structurally normal eye from abnormal visual development (strabismic, refractive/anisometropic or deprivation) during the critical period — reversible ONLY if treated early. The screen and cover test exist to catch it.

Infection of the eyelid and periocular soft tissue ANTERIOR to the orbital septum, without orbital involvement. Presents with a red, swollen, tender lid but — crucially — NORMAL eye movements, NO proptosis and NORMAL vision/colour. Treated with oral antibiotics; the essential skill is distinguishing it from sight- and life-threatening orbital cellulitis.

A sight- and life-threatening infection of the orbital tissues posterior to the septum, usually spreading from ethmoid sinusitis. Presents with a red swollen lid PLUS proptosis, painful/restricted eye movements (ophthalmoplegia), and reduced vision/colour. An emergency: admit for IV antibiotics and CT; complications include abscess, cavernous sinus thrombosis, meningitis and blindness.

A sight-threatening infection of the aqueous and/or vitreous cavities. Most commonly exogenous after intraocular surgery (cataract) or intravitreal injection, or following penetrating trauma; rarely endogenous (haematogenous, e.g. IV drug use, sepsis, candidaemia). Presents days after surgery with pain, dramatic visual loss and a hypopyon — an emergency requiring vitreous sampling and intravitreal antibiotics.

Reactivation of varicella-zoster virus in the ophthalmic (V1) division of the trigeminal nerve. A painful vesicular dermatomal rash of the forehead/upper lid that may threaten the eye. Hutchinson sign (vesicles on the nose tip — nasociliary nerve) predicts ocular involvement. Treated with oral/IV antivirals; ocular involvement needs ophthalmology.

Autoimmune inflammation and expansion of the orbital fat and extraocular muscles associated with Graves disease (can occur euthyroid/hypothyroid). Causes proptosis, lid retraction, restrictive diplopia and ocular-surface exposure; the sight-threatening complication is compressive (dysthyroid) optic neuropathy. Smoking markedly worsens it. Managed with risk-factor control, selenium, steroids/immunotherapy and orbital decompression.

Chronic keratoconjunctivitis from ocular Chlamydia trachomatis (serovars A–C), spread by flies and close contact in endemic areas with poor sanitation — the leading INFECTIOUS cause of blindness worldwide. Repeated infection scars the conjunctiva (Arlt line), causing cicatricial entropion and trichiasis that abrade the cornea, leading to opacification and blindness. Controlled with the WHO SAFE strategy.

The pattern of field loss localises the lesion with unusual precision, which is why it is examined so often. The single most useful rule: loss in ONE eye only is pre-chiasmal (retina or optic nerve); loss in the SAME half of both visual fields is post-chiasmal (tract, radiation or cortex).